In the medical field, various types of implantable leads are known and used. Particularly in the field of cardiac pulse generators, the use of implanted pacing and/or sensing leads is very common. Implantable cardiac pulse generators are typically implanted either in the region of a patient's thoracic cavity, for example under the skin near the patient's left or right clavicle, or in the patient's abdomen. A pacemaker lead, having a proximal end coupled to the pulse generator and a distal end that is in electrical contact with the patient's heart muscle, functions to convey electrical cardiac signals to sensing circuitry associated with the pulse generator, and/or to convey electrical stimulating pulses (e.g., pacing pulses) to the cardiac muscle from the pulse generator.
Different types of cardiac lead configurations may be required depending upon whether implantation is to be endocardial (i.e., when the lead is transvenously introduced to place the distal end within one of the chambers of the heart) or epicardial (i.e., when the lead is introduced from the outside of the cardiovascular system to bring the distal end in contact with epicardial or myocardial tissue).
Whether a lead is configured for epicardial use or endocardial use, it is important that a mechanically stable and electrically efficient interface between cardiac tissue and the electrode(s) be established. From an electrical perspective, the electrode/tissue interface is typically characterized in terms of its threshold and its impedance. Those of ordinary skill in the art will appreciate that it is desirable to minimize the threshold of the electrode/tissue interface, so that the current drained from the pulse generator batter can be minimized by using lower-level stimulating pulses. On the other hand, it is also desirable to efficiently maximize the impedance of the electrode/tissue interface to additionally minimize the current drain.
It has been shown in the prior art that the impedance of the electrode/tissue interface can be maximized by decreasing the geometric surface area (size) of the stimulating electrode. There is a trade-off, however, between providing a small size electrode and ensuring suitable sensing and low-threshold properties of the electrode. This trade-off is discussed in greater detail in U.S. patent application Ser. No. 08/056,448 filed on Apr. 30, 1993 in the name of James T. Gates and entitled "Substrate for a Sintered Electrode," which application is hereby incorporated herein by reference in its entirety. As noted in the Gates '448 application, a considerable breakthrough in the development of low-threshold, high-impedance electrode technology occurred with the invention of a steroid-eluting porous pacing electrode, as described in U.S. Pat. No. 4,506,680 to Stokes, and related U.S. Pat. Nos. 4,577,642; 4,606,118; and 4,711,251, all commonly assigned to the assignee of the present invention and hereby incorporated by reference herein in their respective entireties.
The electrode disclosed in the Stokes '680 patent is constructed of porous, sintered platinum, titanium, or the like. Proximate the electrode is placed a plug of silicone rubber impregnated with the sodium salt of dexamethasone phosphate or other glucocorticosteroids. The silicone rubber plug allows the release of the steroid through the interstitial gaps in the porous sintered metal electrode to reach the electrode/tissue interface. The eluted steroid mitigates inflammation, irritability and subsequent excessive fibrosis of the tissue adjacent to the electrode itself.
While the steroid-eluting lead described in the Stokes '680 patent represent a significant advancement in the field of low-threshold, high-impedance cardiac leads, the mechanical attributes of the electrode/tissue interface and of the mechanism employed to ensure good fixation and permanent engagement of the lead with cardiac tissue can also have a significant impact on the threshold and impedance characteristics of a lead. Mechanical considerations are particularly relevant in the context of chronically-implanted leads, which are subjected to years of mechanical stresses.
With regard to the fixation mechanism for securing the electrode in a desired position, various approaches have been proposed in the prior art. Such mechanisms fall generally into two categories: passive fixation and active fixation. A well-known example of a passive fixation mechanism is an endocardial lead provided with pliant barbs or "tines" attached at or near the distal tip to engage the trabeculae within the heart chamber. Known active fixation mechanisms include corkscrews, hooks, piercing barbs or other anchoring structures arranged at or near the distal tip for penetration of cardiac tissue upon proper positioning of the electrode.
An example of a lead having a hook-type stab-in fixation mechanism is the Model 4951 lead manufactured by Medtronic, Inc., Minneapolis, Minn. Experimental data suggests that over time, electrodes such as the Model 4951 tend to have the myocardium between the hooked electrode and the epicardial pad replaced with fat. Such fat deposits are believed to be the result of muscle degeneration, probably an effect of the way the tissue beats against the rigid electrode. Hook-type electrodes which angle down into the myocardium (as opposed to the upward angle of the Model 4951) may provoke additional fibrotic damage at and in the tissue distal to the electrode's sharp point. Additionally, such downward-oriented hooks may also provoke fibrotic tracts angling further down under the electrode. Those of ordinary skill in the art will appreciate that such fibrotic and/or fatty deposits tend to reduce the quality of the electrode/tissue interface.
Similar fatty replacement, inflammatory, and fibrotic responses have also been observed for so-called "stab-in" type electrodes (such as the Model 5815 manufactured by Medtronic) and "screw-in" type electrodes (such as the Model 6917A manufactured by Medtronic).
For each of the active-fixation epicardial electrodes discussed above, the electrodes are applied to the epicardial surface of the heart with the electrode in intimate contact with the myocardium and held rigid with respect to the surrounding compliant myocardial tissue. Such rigidity is believed to contribute to the aforementioned fatty-replacement, inflammatory, and fibrotic responses which can result in sub-optimal electrical performance, particularly in long-term implants.